Pear anthracnose,caused by Colletotrichum fructicola,is a devastating disease that seriously affects most pear varieties,compromising their yield and quality.However,effective control of this pathogen is lacking.Moreo...Pear anthracnose,caused by Colletotrichum fructicola,is a devastating disease that seriously affects most pear varieties,compromising their yield and quality.However,effective control of this pathogen is lacking.Moreover,the critical resistance responses to C.fructicola in pear are unknown.To investigate these resistance mechanisms of pear against C.fructicola,transcriptomic and metabolomic analyses were performed on the anthracnose-resistant variety‘Seli’and susceptible variety‘Cuiguan’after C.fructicola infection.Differentially expressed genes(DEGs)and differentially accumulated metabolites(DAMs)were mainly involved in metabolism and secondary metabolite synthetic pathways,includingα-linoleic acid metabolism,phenylalanine biosynthesis metabolism,unsaturated fatty acids biosynthesis,and biosynthesis of amino acids and their derivatives.In particular,the accumulation of unsaturated fatty acids(UFAs),amino acids,and their derivatives,such as linoleic acid and its derivatives,lauric acid,N-acetyl-L-glutamic acid,and L-proline,was significantly increased in‘Seli’after infection,while the amino acids of oxiglutatione and N-acetyl-L-glutamic acid,as well as the proanthocyanidins,were significantly decreased in‘Cuiguan’.These findings suggest that these metabolites may contribute to the differential anthracnose resistance between‘Seli’and‘Cuiguan’.Overall,our results provid new insights into the regulation of pear anthracnose resistance,which may assist in developing new control strategies and breeding anthracnose-resistant varieties.展开更多
The present study was performed mainly to investigate the antagonist-pathogen-host interaction in wounds of the sweet cherry fruits. The antagonistic yeast Cryptococcus laurentii could significantly reduce the brown r...The present study was performed mainly to investigate the antagonist-pathogen-host interaction in wounds of the sweet cherry fruits. The antagonistic yeast Cryptococcus laurentii could significantly reduce the brown rot of the sweet cherry fruit caused by Monilinia fructicola at 25 and 1 ℃. The populations of yeast increased faster in the presence of the pathogen initially, but then decreased rapidly. In the fruits inoculated with M. fructicola alone or combined with C. laurentii, an induction of lipid peroxidation as well as activities of the antioxidant enzymes, such as, superoxide dismutases （SOD）, catalase （CAT）, and peroxidase （POD）, was observed. The isoenzyme pattern of polypheno/oxidase （PPO） changed greatly after the symptoms appeared, with new PPO isoforms being induced. By contrast, the induction of lipid peroxidation and activities of SOD, CAT, and POD were low, although no significant changes were found in the PPO isoenzyms in the fruits inoculated with antagonist C. laurentii alone. The inhibition of brown rot during the antagonist- pathogen-host interaction in wounds of the sweet cherry fruits was mainly on account of the stimulated growth of C. laurentii as well as the induction of antioxidant enzymes of the fruits by M. fructicola.展开更多
Based on the recently published whole-genome sequence of cultivated strawberry ’Camarosa’, in this study, 222FaWRKY genes were identified in the ’Camarosa’ genome. Phylogenetic analysis showed that the 222 FaWRKY ...Based on the recently published whole-genome sequence of cultivated strawberry ’Camarosa’, in this study, 222FaWRKY genes were identified in the ’Camarosa’ genome. Phylogenetic analysis showed that the 222 FaWRKY candidate genes were classified into three groups, of which 41 were in group Ⅰ, 142 were in group Ⅱ, and 39 were in group Ⅲ. The 222 FaWRKY genes were evenly distributed among the seven chromosomes. The exon–intron structures and motifs of the WRKY genes had evolutionary diversity in different cultivated strawberry genomes. Regarding differential expression, the expression of FaWRKY133 was relatively high in leaves, while FaWRKY63 was specifically expressed in roots. FaWRKY207, 59, 46, 182, 156, 58, 39, 62 and 115 were up-regulated during achene development from the green to red fruit transition. FaWRK181, 166 and 211 were highly expressed in receptacles at the ripe fruit stage. One interesting finding was that Fa WRKY179 and 205 were significantly repressed after Colletotrichum fructicola inoculation in both ’Benihoppe’ and ’Sweet Charlie’ compared with Mock. The data reported here provide a foundation for further comparative genomics and analyses of the distinct expression patterns of FaWRKY genes in various tissues and in response to C. fructicola inoculation.展开更多
Monilinia fructicola has been widely reported as the causal agent of brown rot disease on many Rosaceae family fruits worldwide.It has been reported on stone fruits,e.g.,peach,plum,cherry,apricot and mume;as well as p...Monilinia fructicola has been widely reported as the causal agent of brown rot disease on many Rosaceae family fruits worldwide.It has been reported on stone fruits,e.g.,peach,plum,cherry,apricot and mume;as well as pome fruits,e.g.,apple,pear and hawthorn.Loquat is a member of the Eriobotrya genus in subfamily Maloideae along with apple,pear and hawthorn.So far,loquat has not been reported as the host of any Monilia species.In June 2019,brown rot symptoms were observed on loquat fruits in an orchard in Wuhan,Hubei Province,China.Thirty single spore isolates were obtained and identified as M.fructicola based on morphological characteristics and molecular analysis.This is the first report of loquat brown rot disease caused by Monilia species in the world.Furthermore,upon artificial inoculation,all three Monilia species from peach in China,i.e.,M.fructicola,M.mumecola and M.yunnanensis,could cause typical brown rot disease on loquat fruits.At the same time,M.fructicola isolates from loquat showed virulence similar to those isolates from peach when the pathogenicity test was conducted on peach fruits.These results suggested that loquat could be infected by other Monilia species and that isolates from loquat also have potential to damage other Rosaceae family fruits in practice.展开更多
Peach brown rot, caused by Monilinia fructicola, is one of the most serious peach diseases. A strain belonging to the Actinomycetales, named Streptomyces blastmyceticus JZB130180, was found to have a strong inhib-itor...Peach brown rot, caused by Monilinia fructicola, is one of the most serious peach diseases. A strain belonging to the Actinomycetales, named Streptomyces blastmyceticus JZB130180, was found to have a strong inhib-itory effect on M. fructicola in confrontation culture. Following the inoculation of peaches in vitro, it was revealed that the fermentation broth of S. blastmyceticus JZB130180 had a significant inhibitory effect on disease development by M. fructicola. The fermentation broth of S. blastmyceticus JZB130180 had an EC50(concentration for 50% of maximal effect) of 38.3 μg/mL against M. fructicola, as determined in an indoor toxicity test. Analysis of the physicochemical properties of the fermentation broth revealed that it was tolerant of acid and alkaline conditions, temperature, and ultraviolet radiation. In addition, chitinase, cellulase, and protease were also found to be secreted by the strain. The results of this study suggest that S. blastmyceticus JZB130180 may be used for the biocontrol of peach brown rot.展开更多
The Arabidopsis Toxicos en Levadura(ATL)protein is a subfamily of the E3 ubiquitin ligases,which exists widely in plants and is extensively involved in plant growth and development.Although the ATL family has been ide...The Arabidopsis Toxicos en Levadura(ATL)protein is a subfamily of the E3 ubiquitin ligases,which exists widely in plants and is extensively involved in plant growth and development.Although the ATL family has been identified in other species,such as Arabidopsis,Oryza sativa,and grapevine,few reports on pear ATL gene families have been reported.In this study,92 PbrATL genes were identified and analyzed from the Pyrus breschneideri genome.Motif analysis and phylogenetic tree generation divided them into nine subgroups,and chromosome localization analysis showed that the 92 PbrATL genes were distributed in 16 of 17 pear chromosomes.Transcriptome data and quantitative real-time polymerase chain reaction(qRT-PCR)experiments demonstrated that PbrATL18,PbrATL41,and PbrATL88 were involved in both pear drought resistance and Colletotrichum fructicola infection.In addition,Arabidopsis thaliana overexpressing PbrATL18 showed greater resistance to drought stress than the wild type(WT),and PbrATL18-silenced pear seedlings showed greater sensitivity to drought and C.fructicola infection than the controls.PbrATL18 regulated plant resistance by regulating chitinase(CHI),phenylalanine ammonia-lyase(PAL),polyphenol oxidase(PPO),catalase(CAT),peroxidase(POD),and superoxide dismutase(SOD)activities.This study provided a reference for further exploring the functions of the PbrATL gene in drought resistance and C.fructicola infection.展开更多
[Objective]The paper was to compare the indoor toxicities of sixteen fungicides on mycelial growth and spore germination of Monilinia fructicola,to screen out effective fungicides and to discuss use characteristics of...[Objective]The paper was to compare the indoor toxicities of sixteen fungicides on mycelial growth and spore germination of Monilinia fructicola,to screen out effective fungicides and to discuss use characteristics of various types of fungicides.[Method]The inhibitory activities of 16 fungicides on mycelial growth and spore germination were determined by mycelial growth rate method and spore germination method.[Result]The EC50 values of 16 fungicides against mycelial growth ranged from 0.0184 to 61.5305 mg/L.Prochloraz,tetramycin,fenbuconazole and fludioxonil had strong inhibitory activities on mycelial growth,and their EC50 values were 0.0184,0.0456,0.0531 and 0.0814 mg/L,respectively,significantly lower than those of other 12 fungicides.The EC50 values of 16 fungicides against spore germination ranged from 0.0084 to 189.3938 mg/L.Tetramycin and chlorothalonil had strong inhibitory activities on mycelial growth,and their EC50 values were 0.0084 and 0.0378 mg/L,respectively,significantly lower than those of other 14 fungicides.[Conclusion]The 16 fungicides had great value in preventing and controlling peach brown rot.Benzimidazoles,diformimides and ergosterol inhibitors had good inhibitory activities on mycelial growth.Strobilurins,succinate dehydrogenase inhibitors and multiple-site protective fungicides had good inhibitory activities on spore germination.The agricultural antibiotics tetramycin,phenazine-1-carboxylic acid and pyrrole fungicide fludioxonil had good inhibitory activities on mycelial growth and spore germination.展开更多
Pear anthracnose,caused by the fungus Colletotrichum fructicola,is a devastating disease for the pear industry.The apoplast,an extracellular compartment outside the plasma membrane,plays a crucial role in water and nu...Pear anthracnose,caused by the fungus Colletotrichum fructicola,is a devastating disease for the pear industry.The apoplast,an extracellular compartment outside the plasma membrane,plays a crucial role in water and nutrient transport,as well as plant-microbe interactions.This study aimed to uncover the molecular mechanism of pear leaf apoplastic protein-mediated resistance to C.fructicola.Apoplast fluid was isolated using the vacuum infiltration method,and defence-related apoplastic proteins were identified through protein mass spectrometry and transcriptome sequencing.We found 213 apoplastic proteins in the leaf apoplast fluid during early C.fructicola infection,with the majority(74.64%)being enzymes,including glycosidases,proteases,and oxidoreductases.Gene Ontology analysis revealed their involvement in defence response,enzyme inhibition,carbohydrate metabolism,and phenylpropanoid biosynthesis.Transcriptome analysis showed the infection induced expression of certain apoplast proteins,potentially contributing to pear leaf resistance.Notably,the expression of PbrGlu1,an endo-β-1,3-glucanase from the glycoside hydrolase 17 family,was significantly higher in infected leaves.Silencing of the PbrGlu1 gene increased pear leaf susceptibility to C.fructicola,leading to more severe symptoms and higher reactive oxygen species content.Overall,our study provides insights into the apoplast space interaction between pear leaves and C.fructicola,identifies a key gene in infected pears,and offers a foundation and new strategy for understanding the molecular mechanisms underlying pear anthracnose and breeding disease-resistant pears.展开更多
Anthracnose is a common disease found in Camellia oleifera producing areas across China,whose primary pathogen is Colletotrichum fructicola.We previously revealed that autophagy is essential for the pathogenicity of C...Anthracnose is a common disease found in Camellia oleifera producing areas across China,whose primary pathogen is Colletotrichum fructicola.We previously revealed that autophagy is essential for the pathogenicity of C.fructicola.However,the function of ubiquitin–proteasome system(UPS),which is a parallel protein degradation pathway to autophagy,remains elusive.Here,we report that CfRad6,an E2 conjugating enzyme in UPS,interacts with three putative E3 ubiquitin ligases,namely CfRad18,CfUbr1,and CfBre1.Importantly,we presented evidence showing that CfRad6 negatively regulates autophagy,revealing the first link between UPS and autophagy in pathogenic fungi.Targeted gene deletion showed that CfRad6 is involved in growth and conidiation.We further found that theΔCfrad6 mutant is defective in appressoria formation and responses to environmental stresses.These combined effects,along with the abnormal autophagy level,lead to the pathogenicity defects of theΔCfrad6 mutant.Taken together,our study indicates the pleiotropic functions of CfRad6 in the development and pathogenicity of C.fructicola.展开更多
基金supported by the China Agriculture Research System(CARS-28-14)the National Natural Science Foundation of China(32302484)the University Natural Science Research Project of Anhui Province,China(2022AHO50926 and 2022AH040129).
文摘Pear anthracnose,caused by Colletotrichum fructicola,is a devastating disease that seriously affects most pear varieties,compromising their yield and quality.However,effective control of this pathogen is lacking.Moreover,the critical resistance responses to C.fructicola in pear are unknown.To investigate these resistance mechanisms of pear against C.fructicola,transcriptomic and metabolomic analyses were performed on the anthracnose-resistant variety‘Seli’and susceptible variety‘Cuiguan’after C.fructicola infection.Differentially expressed genes(DEGs)and differentially accumulated metabolites(DAMs)were mainly involved in metabolism and secondary metabolite synthetic pathways,includingα-linoleic acid metabolism,phenylalanine biosynthesis metabolism,unsaturated fatty acids biosynthesis,and biosynthesis of amino acids and their derivatives.In particular,the accumulation of unsaturated fatty acids(UFAs),amino acids,and their derivatives,such as linoleic acid and its derivatives,lauric acid,N-acetyl-L-glutamic acid,and L-proline,was significantly increased in‘Seli’after infection,while the amino acids of oxiglutatione and N-acetyl-L-glutamic acid,as well as the proanthocyanidins,were significantly decreased in‘Cuiguan’.These findings suggest that these metabolites may contribute to the differential anthracnose resistance between‘Seli’and‘Cuiguan’.Overall,our results provid new insights into the regulation of pear anthracnose resistance,which may assist in developing new control strategies and breeding anthracnose-resistant varieties.
基金the Knowledge Innovation Program of the Chinese Academy of Sciences, China （KSCX2-YW-G-010）； the National Natural Science Foundation of China （30671473）.
文摘The present study was performed mainly to investigate the antagonist-pathogen-host interaction in wounds of the sweet cherry fruits. The antagonistic yeast Cryptococcus laurentii could significantly reduce the brown rot of the sweet cherry fruit caused by Monilinia fructicola at 25 and 1 ℃. The populations of yeast increased faster in the presence of the pathogen initially, but then decreased rapidly. In the fruits inoculated with M. fructicola alone or combined with C. laurentii, an induction of lipid peroxidation as well as activities of the antioxidant enzymes, such as, superoxide dismutases （SOD）, catalase （CAT）, and peroxidase （POD）, was observed. The isoenzyme pattern of polypheno/oxidase （PPO） changed greatly after the symptoms appeared, with new PPO isoforms being induced. By contrast, the induction of lipid peroxidation and activities of SOD, CAT, and POD were low, although no significant changes were found in the PPO isoenzyms in the fruits inoculated with antagonist C. laurentii alone. The inhibition of brown rot during the antagonist- pathogen-host interaction in wounds of the sweet cherry fruits was mainly on account of the stimulated growth of C. laurentii as well as the induction of antioxidant enzymes of the fruits by M. fructicola.
基金supported by the National Natural Science Foundation of China (31601731)
文摘Based on the recently published whole-genome sequence of cultivated strawberry ’Camarosa’, in this study, 222FaWRKY genes were identified in the ’Camarosa’ genome. Phylogenetic analysis showed that the 222 FaWRKY candidate genes were classified into three groups, of which 41 were in group Ⅰ, 142 were in group Ⅱ, and 39 were in group Ⅲ. The 222 FaWRKY genes were evenly distributed among the seven chromosomes. The exon–intron structures and motifs of the WRKY genes had evolutionary diversity in different cultivated strawberry genomes. Regarding differential expression, the expression of FaWRKY133 was relatively high in leaves, while FaWRKY63 was specifically expressed in roots. FaWRKY207, 59, 46, 182, 156, 58, 39, 62 and 115 were up-regulated during achene development from the green to red fruit transition. FaWRK181, 166 and 211 were highly expressed in receptacles at the ripe fruit stage. One interesting finding was that Fa WRKY179 and 205 were significantly repressed after Colletotrichum fructicola inoculation in both ’Benihoppe’ and ’Sweet Charlie’ compared with Mock. The data reported here provide a foundation for further comparative genomics and analyses of the distinct expression patterns of FaWRKY genes in various tissues and in response to C. fructicola inoculation.
基金financially supported by the earmarked fund for China Agriculture Research System(CARS-30)the National Natural Science Foundation of China(31401686 and 31872934)。
文摘Monilinia fructicola has been widely reported as the causal agent of brown rot disease on many Rosaceae family fruits worldwide.It has been reported on stone fruits,e.g.,peach,plum,cherry,apricot and mume;as well as pome fruits,e.g.,apple,pear and hawthorn.Loquat is a member of the Eriobotrya genus in subfamily Maloideae along with apple,pear and hawthorn.So far,loquat has not been reported as the host of any Monilia species.In June 2019,brown rot symptoms were observed on loquat fruits in an orchard in Wuhan,Hubei Province,China.Thirty single spore isolates were obtained and identified as M.fructicola based on morphological characteristics and molecular analysis.This is the first report of loquat brown rot disease caused by Monilia species in the world.Furthermore,upon artificial inoculation,all three Monilia species from peach in China,i.e.,M.fructicola,M.mumecola and M.yunnanensis,could cause typical brown rot disease on loquat fruits.At the same time,M.fructicola isolates from loquat showed virulence similar to those isolates from peach when the pathogenicity test was conducted on peach fruits.These results suggested that loquat could be infected by other Monilia species and that isolates from loquat also have potential to damage other Rosaceae family fruits in practice.
基金Project supported by the Beijing Municipal Science and Technology Plan Projects(No.D151100003915002)the Special Project for Innovation Ability Construction from the Beijing Academy of Agriculture and Forestry Sciences(No.KJCX20170415)+2 种基金the Beijing Agriculture Innovation Consortium(No.BAIC07-2018)the Science and Technology Innovation Ability Construction Fund from the Beijing Academy of Agriculture and Forestry Sciences(No.KJCX20170107)the Science and Technology Innovation Team of the Beijing Academy of Agriculture and Forestry Sciences(No.JNKST201607),China
文摘Peach brown rot, caused by Monilinia fructicola, is one of the most serious peach diseases. A strain belonging to the Actinomycetales, named Streptomyces blastmyceticus JZB130180, was found to have a strong inhib-itory effect on M. fructicola in confrontation culture. Following the inoculation of peaches in vitro, it was revealed that the fermentation broth of S. blastmyceticus JZB130180 had a significant inhibitory effect on disease development by M. fructicola. The fermentation broth of S. blastmyceticus JZB130180 had an EC50(concentration for 50% of maximal effect) of 38.3 μg/mL against M. fructicola, as determined in an indoor toxicity test. Analysis of the physicochemical properties of the fermentation broth revealed that it was tolerant of acid and alkaline conditions, temperature, and ultraviolet radiation. In addition, chitinase, cellulase, and protease were also found to be secreted by the strain. The results of this study suggest that S. blastmyceticus JZB130180 may be used for the biocontrol of peach brown rot.
基金supported by the National Key Research and Development Program of China(Grant No.2022YFD1200503)Jiangsu Agriculture Science and Technology Innovation Fund[Grant No.CX(22)3046]+2 种基金the National Science Foundation of China(Grant No.32072538)the Project Funded by the Priority Academic Program Development of Jiangsu Higher Education Institutionsthe Earmarked Fund for China Agriculture Research System(Grant No.CARS-28).
文摘The Arabidopsis Toxicos en Levadura(ATL)protein is a subfamily of the E3 ubiquitin ligases,which exists widely in plants and is extensively involved in plant growth and development.Although the ATL family has been identified in other species,such as Arabidopsis,Oryza sativa,and grapevine,few reports on pear ATL gene families have been reported.In this study,92 PbrATL genes were identified and analyzed from the Pyrus breschneideri genome.Motif analysis and phylogenetic tree generation divided them into nine subgroups,and chromosome localization analysis showed that the 92 PbrATL genes were distributed in 16 of 17 pear chromosomes.Transcriptome data and quantitative real-time polymerase chain reaction(qRT-PCR)experiments demonstrated that PbrATL18,PbrATL41,and PbrATL88 were involved in both pear drought resistance and Colletotrichum fructicola infection.In addition,Arabidopsis thaliana overexpressing PbrATL18 showed greater resistance to drought stress than the wild type(WT),and PbrATL18-silenced pear seedlings showed greater sensitivity to drought and C.fructicola infection than the controls.PbrATL18 regulated plant resistance by regulating chitinase(CHI),phenylalanine ammonia-lyase(PAL),polyphenol oxidase(PPO),catalase(CAT),peroxidase(POD),and superoxide dismutase(SOD)activities.This study provided a reference for further exploring the functions of the PbrATL gene in drought resistance and C.fructicola infection.
基金Major Science and Technology Innovation Project of Shandong Province(2018CXGC0213).
文摘[Objective]The paper was to compare the indoor toxicities of sixteen fungicides on mycelial growth and spore germination of Monilinia fructicola,to screen out effective fungicides and to discuss use characteristics of various types of fungicides.[Method]The inhibitory activities of 16 fungicides on mycelial growth and spore germination were determined by mycelial growth rate method and spore germination method.[Result]The EC50 values of 16 fungicides against mycelial growth ranged from 0.0184 to 61.5305 mg/L.Prochloraz,tetramycin,fenbuconazole and fludioxonil had strong inhibitory activities on mycelial growth,and their EC50 values were 0.0184,0.0456,0.0531 and 0.0814 mg/L,respectively,significantly lower than those of other 12 fungicides.The EC50 values of 16 fungicides against spore germination ranged from 0.0084 to 189.3938 mg/L.Tetramycin and chlorothalonil had strong inhibitory activities on mycelial growth,and their EC50 values were 0.0084 and 0.0378 mg/L,respectively,significantly lower than those of other 14 fungicides.[Conclusion]The 16 fungicides had great value in preventing and controlling peach brown rot.Benzimidazoles,diformimides and ergosterol inhibitors had good inhibitory activities on mycelial growth.Strobilurins,succinate dehydrogenase inhibitors and multiple-site protective fungicides had good inhibitory activities on spore germination.The agricultural antibiotics tetramycin,phenazine-1-carboxylic acid and pyrrole fungicide fludioxonil had good inhibitory activities on mycelial growth and spore germination.
基金supported by the Research and Development Program of China(2022YFF1003100-02)the National Natural Science Foundation of China(31830081,32172511)+4 种基金the Jiangsu Agriculture Science and Technology Innovation Fund(CX(22)2025)the Seed Industry Promotion Project of Jiangsu(JBGS(2021)022)the Guidance Foundation of the Hainan Institute of Nanjing Agricultural University(NAUSY-MS08)the Project Funded by the Priority Academic Program Development of Jiangsu Higher Education Institutions,and the Earmarked Fund for China Agriculture Research System(CARS-28)supported by the High-performance Computing Platform of the Bioinformatics Center,Nanjing Agricultural University.
文摘Pear anthracnose,caused by the fungus Colletotrichum fructicola,is a devastating disease for the pear industry.The apoplast,an extracellular compartment outside the plasma membrane,plays a crucial role in water and nutrient transport,as well as plant-microbe interactions.This study aimed to uncover the molecular mechanism of pear leaf apoplastic protein-mediated resistance to C.fructicola.Apoplast fluid was isolated using the vacuum infiltration method,and defence-related apoplastic proteins were identified through protein mass spectrometry and transcriptome sequencing.We found 213 apoplastic proteins in the leaf apoplast fluid during early C.fructicola infection,with the majority(74.64%)being enzymes,including glycosidases,proteases,and oxidoreductases.Gene Ontology analysis revealed their involvement in defence response,enzyme inhibition,carbohydrate metabolism,and phenylpropanoid biosynthesis.Transcriptome analysis showed the infection induced expression of certain apoplast proteins,potentially contributing to pear leaf resistance.Notably,the expression of PbrGlu1,an endo-β-1,3-glucanase from the glycoside hydrolase 17 family,was significantly higher in infected leaves.Silencing of the PbrGlu1 gene increased pear leaf susceptibility to C.fructicola,leading to more severe symptoms and higher reactive oxygen species content.Overall,our study provides insights into the apoplast space interaction between pear leaves and C.fructicola,identifies a key gene in infected pears,and offers a foundation and new strategy for understanding the molecular mechanisms underlying pear anthracnose and breeding disease-resistant pears.
基金funded by the National Natural Science Foundation of China(32001317).
文摘Anthracnose is a common disease found in Camellia oleifera producing areas across China,whose primary pathogen is Colletotrichum fructicola.We previously revealed that autophagy is essential for the pathogenicity of C.fructicola.However,the function of ubiquitin–proteasome system(UPS),which is a parallel protein degradation pathway to autophagy,remains elusive.Here,we report that CfRad6,an E2 conjugating enzyme in UPS,interacts with three putative E3 ubiquitin ligases,namely CfRad18,CfUbr1,and CfBre1.Importantly,we presented evidence showing that CfRad6 negatively regulates autophagy,revealing the first link between UPS and autophagy in pathogenic fungi.Targeted gene deletion showed that CfRad6 is involved in growth and conidiation.We further found that theΔCfrad6 mutant is defective in appressoria formation and responses to environmental stresses.These combined effects,along with the abnormal autophagy level,lead to the pathogenicity defects of theΔCfrad6 mutant.Taken together,our study indicates the pleiotropic functions of CfRad6 in the development and pathogenicity of C.fructicola.
